The DIP2A Knockout K-562 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the DIP2A gene in the K-562 human chronic myelogenous leukemia (CML) suspension cell line. This heterogeneous loss-of-function model avoids clonal artifacts and is designed for studying DIP2A-dependent signaling and cellular phenotypes. Disruption of DIP2A abrogates downstream pro-survival pathways, providing a valuable tool for oncogenic signaling analysis and functional genomics studies.
K-562 cells originate from a CML blast crisis patient and harbor the BCR-ABL fusion oncogene, displaying an undifferentiated blast phenotype and exhibiting high proliferative capacity in suspension culture. This cell line is extensively used to investigate BCR-ABL-driven oncogenesis, drug sensitivity, and imatinib resistance, serving as a classical model for tyrosine kinase inhibitor response. The leukemic background offers a relevant context for assessing DIP2A’s role in myeloid malignancies.
DIP2A acts as a receptor for follistatin-like 1 (FSTL1), activating Akt/mTOR signaling. FSTL1 binding triggers Akt phosphorylation, leading to mTOR activation and downstream phosphorylation of p70S6K and 4E-BP1. This cascade upregulates Bcl-2 and survivin while inhibiting caspase-3, promoting cell survival and anti-apoptosis. DIP2A interacts with integrin ??1 and is regulated by the transcription factor Sp1. In cancer, DIP2A overexpression drives proliferation and chemoresistance, while knockout suppresses tumor growth. The FSTL1?CDIP2A?CAkt?CmTOR axis is also involved in neuronal development, angiogenesis, and cardiovascular disease.
In K-562 leukemia cells, DIP2A likely sustains survival signaling and may influence sensitivity to imatinib and other chemotherapeutic agents. Knockout of DIP2A in this BCR-ABL-positive model enables dissection of its contribution to leukemic cell viability, clonogenic growth, and drug response. Since DIP2A is implicated in gastric cancer, glioblastoma, and other malignancies, the knockout cells serve as a comparative model for studying shared oncogenic mechanisms and leukemia-specific pathway dependencies.
This product is applicable to functional studies of DIP2A in leukemia, investigation of FSTL1?CDIP2A signaling, and drug resistance research. Key assays include Western blot for p-Akt, mTOR, Bcl-2, and cleaved caspase-3; Annexin V apoptosis assays; MTT viability; phospho-signaling analysis; RT-qPCR; co-immunoprecipitation for FSTL1-DIP2A interaction; and imatinib sensitivity testing. Researchers can use these cells for therapeutic target validation and chemoresistance studies in CML. For further details, contact Ascent Research.
